PERIPHERAL NERVE INJURY (PNI) - LOWER EXTREMITY

NEUROANATOMY

Three Layers of Connective Tissue around the Nerve:

● Endoneurium: contains the axon and Schwann cell in a grouped arrangement.
● Mesoneurium: supports the capillary network that supplies the nerve fibers. It is eas-
ily compromised and this accounts for the peripheral nerve’s susceptibility to is-
chemia.
● Epineurium: is a loose collection of collagen and elastin fibers that support the facsicles of a
peripheral nerve.

Lumbar Plexus
● Iliohypogastric Nerve
o Roots: L1 (with contributions from T12).
o Motor Functions: Innervates the internal
oblique and transversus abdominis.
o Sensory Functions: Innervates the posterolateral
gluteal skin in the pubic region
● Ilioinguinal Nerve
o Roots: L1.
o Motor Functions: Innervates the internal
oblique and transversus abdominis.
o Sensory Functions: Innervates the skin on the
superior antero-medial thigh. In males, it also
supplies the skin over the root of the penis and
anterior scrotum. In females, it supplies the
skin over mons pubis and labia majora.
● Genitofemoral Nerve
o Roots: L1, L2.
o Motor Functions: The genital branch innervates the
cremasteric muscle.
o Sensory Functions: The genital branch innervates the skin of the anterior scrotum (in
males) or the skin over mons pubis and labia majora (in females). The femoral
branch innervates the skin on the upper anterior thigh.
● Lateral Cutaneous Nerve of the Thigh
o Roots: L2, L3
o Motor Functions: None.
o Sensory Functions: Innervates the anterior and lateral thigh down to the level of the
knee.
● Obturator Nerve
o Roots: L2, L3, L4.
o Motor Functions: Innervates the muscles of the medial thigh – the obturator externus,
adductor longus, adductor brevis, adductor magnus and gracilis.
o Sensory Functions: Innervates the skin over the medial thigh.
● Femoral Nerve
o Roots: L2, L3, L4.
o Motor Functions: Innervates the muscles of the anterior thigh – the illiacus, pectineus,
sartorius and quadriceps femoris.
o Sensory Functions: Innervates the skin on the anterior thigh and the medial leg.
Sacral Plexus
● Superior Gluteal Nerve
o Roots: L4, L5, S1.
o Motor Functions: Innervates the gluteus
minimus, gluteus medius and tensor fascia
lata.
o Sensory Functions: None.
● Inferior Gluteal Nerve
o Roots: L5, S1, S2.
o Motor Functions: Innervates gluteus
maximus.
o Sensory Functions: None.
● Sciatic Nerve
o The sciatic nerve is derived from the lum-
bosacral plexus. After its formation, it
leaves the pelvis and enters the gluteal re-
gion via greater sciatic foramen. It
emerges inferiorly to the piriformis mus-
cle and descends in an inferolateral direc-
tion.
o Roots: L4, L5, S1, S2, S3
o Motor Functions:
▪ Tibial portion – Innervates the
muscles in the posterior
compartment of the thigh (apart from the short head of the biceps femoris),
and the hamstring component of adductor magnus. Innervates all the muscles
in the posterior compartment of the leg and sole of the foot.
▪ Common fibular portion – Short head of biceps femoris, all muscles in the
anterior and lateral compartments of the leg and extensor digitorum bre-
vis.
o Sensory Functions:
▪ Tibial portion: supplies the skin of the posterolateral leg, lateral foot and the
sole of the foot.
▪ Common fibular portion: supplies the skin of the lateral leg and the dorsum
of the foot.
● Posterior Femoral Cutaneous
o Roots: S1, S2, S3
o Motor Functions: None
o Sensory Functions: Innervates the skin on the posterior surface of the thigh and
leg. Also innervates the skin of the perineum.
● Pudendal Nerve
o Roots: S2, S3, S4
o Motor Functions: Innervates the skeletal muscles in the perineum, the external ure-
thral sphincter, the external anal sphincter, levator ani.
o Sensory Functions: Innervates the penis and the clitoris and most of the skin of
the perineum.

DEFINITION
● Peripheral nerve injury is a disorder or disability of a nerve to conduct impulses due to
the disruption in the continuity of the nerve secondary to trauma or disease process.
● Peripheral nerve injuries may result in loss of motor function, sensory function, or both.
Such injuries may occur as a result of trauma (blunt or penetrating) or acute compression.
EPIDEMIOLOGY

Incidence
● The frequency of the lower extremity nerve injuries is assessed to approximately 20 to 23%
of the overall lesions to the peripheral nerve system.
● Peroneal division neuropathy is the most common lower extremity nerve palsy
● The most common cause of PNI was direct laceration from a sharp object (61%)
● Peroneal Nerve: most common site compression is behind the fibular head.
● Tibial Nerve: most common entrapment of the tibial nerve occurs at the tarsal tun-
nel. Age/ Gender
● It affects all ages but older people are more prone.
● The male to female ratio was 2.4:1 (M>F)

ETIOLOGY
● Traumatic (usually caused by a blunt or penetrating trauma)
o Compression
o Crush Injury
o Laceration
o Stretch/ Traction
o Fracture
● Non- Traumatic
o Genetics/ hereditary
o Toxic: results from exposure to a variety of organic and inorganic toxins, medications,
and heavy metals.
o B vitamins deficiency
o Endocrine: diabetes, thyroid or parathyroid
o Viral infection: human immunodeficiency virus (HIV), cytomegalovirus, Epstein-
Barr virus, herpes zoster, Hepatitis C, poliomyelitis, parvovirus, and rabies.
o Bacterial infection: Lyme disease, leprosy, and diphtheria.

Specific Nerve Injury Affectations:

● Sciatic Nerve Injury
o Causes: fracture dislocation of the hip, gunshot wounds, femur fracture
● Common Peroneal Nerve Injury
o Causes: trauma, prolonged crossed legs position, overtight plaster casts applied for
leg fractures
● Tibial Nerve Injury
o Causes: trauma- dislocation of the knee, tarsal tunnel syndrome, laceration injury
● Femoral Nerve Injury
o Causes: injured by a stab and gunshot wounds, pelvic fracture, diabetes, pro-
longed lithotomy position during surgery
TYPES/ CLASSIFICATIONS

There are three basic types of peripheral nerve injuries (PNI) commonly seen in the clinic:
1. Stretch related- the peripheral nerves are elastic, but when a traction force is too strong in-
jury occurs
2. Lacerations- another common type of PNI are lacerations created by blades.

3. Compressions- these injuries include the Saturday Night palsy due to radial nerve com-
pression as well as entrapment neuropathies and do not involve tearing of the neural el-
ements.

SUNDERLAND PROCESS SEDDON

First degree Local myelin damage Neuropraxia

usually secondary to
compression

Second degree Axon damaged; Axonotmesis

endoneurium in-
tact

Third degree Axon, endoneurium Axonotmesis

damaged; perineurium
intact

Fourth degree Axon, endoneurium, Axonotmesis

perineurium damaged;
epineurium intact

Fifth degree Loss of continuity of Neurotmesis

the entire nerve trunk
V. PATHOPHYSIOLOGY

Hallmark: Wallerian Degeneration

(+) Etiologic Factors

Nerve injury

Wallerian degeneration

Macrophages incorporated by Schwann cells will digest the debris

Schwann cells will respond to the loss of axon

Sprouting of axons toward the regeneration tube

Regeneration
Degeneration

● Primary, or retrograde, degeneration is a consequence of trauma and is less common than

secondary (Wallerian) degeneration. The degenerative process proceeds from the site of in-
jury to the next proximal node of Ranvier.
● Secondary or Wallerian degeneration is antegrade, progressing distally from the point of in-
jury. Wallerian degeneration begins on the second or third day after injury, with retraction of
myelin. Nerve fragmentation on day 2 to 3 precedes neurofibrillar degeneration. The nerve
body swells. Neuron edema continues for 10 to 20 days. These changes are more pro-
nounced and longer lasting with proximal nerve lesions. The Schwann cells at the site of in-
jury activate and, by the end of the first week after injury, participate in the removal of myelin
debri.

Regeneration
● Regeneration begins within 24 hours of injury at the proximal end of the injured nerve only if
the endoneurial tube filled with Schwann cells is intact; the axonal sprouts readily pass
across the site of injury.
● The rate of nerve regeneration is 1 mm per day.
● When endoneurial tube is not intact, the many growing sprouts from the axonal stump mi-
grate aimlessly into the epineurium, perineurium and into the adjacent area of to form end
neuroma.
● When proximal end of the nerve is widely separated from the distal end, it may result in
the formation of an end neuroma.
● When nerve is suffered only a partial cut, it results in the formation of a side neuroma.

CLINICAL MANIFESTATIONS
● Tingling, burning or stabbing pain in their feet.
● Sensory changes or loss
● Motor weakness in the distribution of the involved nerve fibers.
● Pain during activities that shouldn't cause pain, such as pain in your feet when putting
weight on them or when they're under a blanket.
● Lack of coordination and falling
● Muscle atrophy

SECONDARY COMPLICATIONS
● Charcot foot
● Loss bowel or bladder function
● Gangrene and amputations

DIAGNOSIS
● History and physical exam:
▪ Deep Tendon Reflexes
 ▪ Manual Muscle Testing
● Sensory Testing:
▪ Light touch can be tested with a cotton.
▪ Vibration sense is tested with a vibrating tuning fork placed over bony prominences
of the feet (ankles)
▪ Test position sense by moving the toe up and down, held by its sides, and have
the patient report its position with eyes closed.
▪ Test pain sense with a blunted, disposable safety pin or splintered cotton tip applicator
● Diagnostic Tests:
o Electromyography (EMG): In an EMG, a thin-needle electrode inserted into your mus-
cle records your muscle's electrical activity at rest and in motion. Reduced muscle ac-
tivity can indicate nerve injury.
o Nerve conduction study: Electrodes placed at two different points in your body
measure how well electrical signals pass through the nerves.
o Magnetic resonance imaging (MRI): MRI uses a magnetic field and radio waves
to produce detailed images of the area affected by nerve damage.
● Special Tests:
o Prone Knee Bending (Nachlas) Test
▪ Positive: Radicular pain to the anterior thigh
▪ Indication: L2- L3 nerve root lesion
o Straight Leg Raise
▪ Positive: Radiating pain on the thigh and leg
▪ Indication: Sciatic nerve neuropathy
o Slump Test
▪ Positive: If the patient is unable to extend the knee because of pain, the
examiner reduces pressure on cervical spine by asking the patient to
slowly raise the head. This test is positive if the patient then able to ex-
tend knee further without/ with less pain.
▪ Indication: affectation of neural structures/ impingement of sciatic nerve

PROGNOSIS

Axonotmesis -Good for healing if short or distal MEDICAL

Class Prognosis
motor or sensory segments are af-
fected
Neuropraxia -Healing in 1–2 months
-Recovery is incomplete—surgical
-Recovery is usually complete
intervention may be required

Neurotmesis -Poor, even with surgery

-No recovery without surgery—re-
covery depends on surgical inter-
vention and correct regrowth of in-
dividual nerve fibers in
endoneural tubes
MANAGEMENT
● NSAIDS: Diclofenac sodium (DS), one of these NSAIDs, has a high specificity for arachi-
donic acid-degrading cyclooxygenase (COX)-2 enzymes. This drug can be used to relieve
neuropathic pain.
● Tricyclic Antidepressants (Amitriptyline): Tricyclic antidepressants are a class of medica-
tions used in the management and treatment of major depressive disorder.
● Serotonin- norepinephrine reuptake inhibitors: SNRIs are used to treat conditions, such
as anxiety disorders and long-term (chronic) pain, especially nerve pain.
● Corticosteroid injection: epidural corticosteroid (steroid) injection is a way to deliver
pain medicine quickly into the body with a syringe.

SURGICAL MANAGEMENT
● Nerve grafts: surgical technique in which a segment of an unrelated nerve is used to re-
place or bridge an injured portion of another nerve.
● Nerve transfer surgery: involves taking nerve branches from a neighboring nerve
and redirecting them to the distal end of the injured nerve.
● Nerve decompression: used to treat peripheral nerve entrapment conditions. The proce-
dure involves removal of the structures that compress on the nerves

PT MANAGEMENT
● Acute Phase
o Movement: Begin range of motion (ROM) to minimize joint and connective con-
tractures and adhesions. This is dictated by the surgeon and type of surgery.
o Splinting or bracing: Splinting or bracing may be necessary to prevent deformities due
to strength imbalances (a plantarflexion splint to prevent foot drop) and to prevent
undue stress on the healing nerve tissue.
o Patient education: Teach the patient safe movements and ways to protect the
extremity to avoid injury due to loss of sensation.
● Recovery Phase
o Motor retraining: When signs of volutional muscle contraction occur, position the
muscle in its shortened position; then ask the patient to hold. Provide assistance
as needed to prevent the part from ―falling‖ out of the shortened position.
▪ Use electrical stimulation to reinforce this active effort.

▪ When the muscles demonstrate control of some range, begin gravity-elimi-

nated, active-assistive ROM. Continue to protect the weak muscles with a
splint or brace.

o Desensitization: As nerves regenerate, the person experiences increased sensitivity

(hypersensitivity) in the area that had previously been without sensation. Use a
graded series of modalities and procedures to decrease the irritability and increase
sensory awareness.
o Discriminative sensory re-education: This is the process of retraining the brain to
recognize a stimulus once the hypersensitivity diminishes.
o Patient education: Instruct the patient to resume use of the extremity gradually while
monitoring pain, swelling, or any discoloration; if necessary, modify or temporarily
avoid any aggravating activities. While the nerve is recovering or if nerve recovery is
incomplete, teach the patient preventive care to avoid injury.
 ● Chronic Phase
o When the potential for reinnervation has peaked and there are minimal or no signs of
reinnervation, emphasize training for compensatory function. The person will proba-
bly have to continue to wear the supportive splint or brace, and preventive care must
continue indefinitely.

Modalities:
● Transcutaneous electrical nerve stimulation (TENS): is a non-invasive, inexpensive,
self- administered technique to relieve pain.
● Functional electrical stimulation (FES): is a technique that uses electrical current to cause a
muscle to contract.

Assistive Devices:
● Handrails
● Canes
● Walker
● Wheel chair

REFERENCES:
Colby & Kisner Therapeutic Exercise 6th Edi-
tion Joel A. De Lisa. Physical Medicine and Rehabilitation Principles and
Practice.
2005. 4th Edition, Volume 1 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6664834/
PERIPHERAL NERVE INJURY (PNI)
UPPER EXTREMITY
 VI. ANATOMY

Peripheral nerve components include the cell body, axons, dendrites, cell membrane, endoneurium,
perineurium, epineurium and schwann cell.
· Axolemma - surface membrane of axon
· Endoneurium - connective tissue which sur-
rounds each axon
· Perineurium - surrounds each fascicle
· Epineurium - surrounds entire nerve fiber
· Schwann cell - lies between the axolemma and
endoneurium which forms myelin and functions to
insulate the axon as well as speed the conduction
of action potentials along the nerve fiber.
Peripheral nerves contain a mix of motor, sensory, and sympathetic neurons:
· Alpha Motor Neurons (somatic efferent fibers): cell bodies located in the anterior column
of spinal cord; innervate skeletal muscles.
· Gamma Motor Neurons (efferent fibers): cell bodies located in lateral columns of spinal
cord; innervate intrafusal muscle fibers of the muscle spindle.
· Sensory Neurons (somatic afferent fibers): cell bodies located in the dorsal root gan-
glia; innervate sensoryreceptors.
· Sympathetic Neurons (visceral afferent fibers): cell bodies located in sympathetic gan-
glia; innervates sweatglands, blood vessels, viscera, and glands.

BRACHIAL PLEXUS

· The brachial plexus terminates in five primary peripheral nerves that are responsible for in-
nervating the tissues of the upper extremity: (1) musculocutaneous, (2) axillary, (3) median,
(4) ulnar, and (5) radial nerves.
· Axillary Nerve (C5, 6): The axillary nerve emerges from the posterior cord of the brachial
plexus; it passes laterally through the axilla, sends a branch to the teres minor muscle,
courses behind the surgical neck ofthe humerus, and innervates the deltoid muscle and
overlying skin.
· Musculocutaneous Nerve (C5, 6): The musculocutaneous nerve emerges from the lateral cord
of the brachial plexus and crosses the axilla with the median nerve; it pierces and innervates
 the coracobrachialis and then travels distally to innervate the biceps and brachialis muscles.
It continues between these muscles to the flexor surface of the elbow; after emerging from
the deep fascia at the elbow, it becomes the lateral cutaneous nerveof the forearm.
· Median Nerve (C5-T1): The median nerve courses the medial aspect of the humerus to the
elbow, where it is deep in the cubital fossa under the bicipital aponeurosis, medial to the
tendon of the biceps and brachial artery; it then moves into the forearm between the two
heads of the pronator teres muscle.
· Ulnar Nerve (C8-T1): The ulnar nerve (Fig. 13.6) emerges from the medial cord of the
brachial plexus at the lower border of the pectoralis minor and descends the arm along the
medial side of the humerus. It passes posterior to the elbow joint in the groove between the
medial epicondyle of the humerus and the olecranon of the ulna. The groove is covered by a
fibrous sheath, which forms the cubital tunnel.
· Radial Nerve (C5-T1): The radial nerve (Fig. 13.7) emerges directly from the posterior cord of
the brachial plexus at the lower border of the pectoralis minor. As it descends the arm, it
winds around the posterior aspect of the humerus in the musculospiral groove and continues
to the radial aspect of the elbow. In the arm it innervates the triceps, anconeus, and upper
portion of the extensor and supinator group of the forearm.

VII. DEFINITION
➢ PNI is a disorder or disability of a nerve to conduct impulses due to the disruption in the
continuity of nerve secondary to trauma or disease process

VIII. EPIDEMIOLOGY
✓ PNI can occur in almost all ages
✓ Nerve injury to the upper extremity is more common than in the lower extremity.
✓ Median nerve is more commonly entrapped at the wrist (CTS); more common in women;
occurs bilaterally in about 50% of cases.
✓ Ulnar nerve is the second most commonly entrapped.
✓ Radial nerve is more commonly injured/fractured
✓ Brachial plexus is the frequent site of traumatic injury
✓ Traumatic neuropathies were more frequent in young males after road accident in upper
limbs.

IX. ETIOLOGY
✓ Trauma
✓ Childbirth injuries
✓ Compression
✓ Lacerations ( a cut or tear in the nerve tissue)
✓ Stretch (traction)
SEDDON AND SUNDERLAND’S CLASSIFICATION OF NERVE INJURY

st
✓ Neuropraxia (1 degree)

▪ Demyelination
▪ Reverse conduction block
▪ Result of mild ischemia from nerve
compression or traction
▪ Recovery is usually complete (minutes
to days)

nd
✓ Axonotmesis (2 degree)
▪ Demyelination + Axonal loss
▪ Wallerian degeneration distal to lesion
▪ Muscle fiber atrophy and sensory loss
▪ Result of prolonged compression or stretch
causing infarction and necrosis
▪ Recovery time precedes at a rate of
about 1mm/day

▪ Complete transection of nerve

 ▪ Muscle fiber atrophy and sensory loss
▪ Result of gunshot or stab wounds
rd th th
▪ No recovery without surgery
▪ Neurotmesis (3 , 4 , 5 )

✓
X. PATHOPHYSIOLOGY

Hallmark: Wallerian Degeneration

(+) Etiologic Factors

Nerve injury

Wallerian degeneration

Macrophages incorporated by Schwann cells will digest the debris

Schwann cells will respond to the loss of axon

Sprouting of axons toward the regeneration tube

Regeneration
 Regeneration

XI. CLINICAL MANIFESTATION

General Signs and Symptoms:
o Flaccidity- because of damage in the Motor nerves. These nerves regulate all the mus-
cles under your conscious control, such as walking, talking, and holding objects.
o Areflexia- It's generally a symptom of peripheral neuropathy, which is damage to a nerve in
the peripheral nervous system.
o Atrophy/Muscle wasting- Damage to the nerves can make it harder to control muscles. It
can also cause weakness. You may notice problems moving a part of your body. You may fall
because your legs buckle.
o Numbness/weakness/paresthesia- Peripheral neuropathy, a result of damage to the nerves
located outside of the brain and spinal cord (peripheral nerves), often causes weakness,
numbness and pain, usually in the hands and feet. It can also affect other areas and body
functions including digestion, urination and circulation.

UPPER EXTREMITY NERVE INJURIES:

➢ Long Thoracic Nerve Injury (C5,6,7)
▪ Serratus Anterior
▪ cause: Traction injury; compression; overuse injury
▪ primary fxn loss: Difficulty elevating the arm; medial winging of scapula; aching/burn-
ing around SH or scapula
▪ “SA palsy/Backpackers Palsy” “Medial winging of scapula”

➢ Thoracic Outlet Syndrome (TOS)

▪ Cause: compressive neuropathy
▪ Pain; paresthesia of medial arm and hand; UE fatigue; Muscle atrophy
▪ cause: excessive SH girdle depression; overly developed trapezius and neck mm; pro-
longed wear of heavy body armor

➢ Axillary Nerve Injury (C5,6)

▪ Deltoid & Teres Minor
▪ cause: acute anterior SH dislocation/reduction; Fx of surgical neck of humerus
▪ primary fxn loss: weakness in SH abduction and lateral rotation
▪ deformity: “Square Shoulder” (from deltoid mm atrophy)

➢ Musculocutaneous Nerve Injury (C5,6,7)

▪ Biceps brachii; Brachialis; Coracobrachialis
▪ primary fxn loss: weakness in elbow flexion with FA supinated
▪ deformity: “Atrophy (flatness) along flexor surface of U.arm”
 ➢ Median Nerve Injury (C5 - T1)
▪ Forearm: PT; PL; FDP; FCR; FDS; FPL; PQ; Wrist and Hand: OP; APB; FPB; Lumbricals I&II
▪ cause: impingement in hypertrophied PT; compression in Carpal Tunnel
▪ primary fxn loss: absent FA pronation, weak grip; no thumb abduction and opposition
therefore unable to do tip-to-tip, tip-to-pad, pad-to-pad prehension
▪ deformity: “Ape Hand” “Carpal Tunnel Syndrome”

➢ Ulnar Nerve Injury (C8 - T1)

▪ Forearm: FCU & FDP; Wrist and Hand: FDM; ODM; AbdDM; Lumbricals III&IV; Interossei;
AP; FPB
▪ cause: compression in Tunnel of Guyon (wrist) & Cubital Tunnel (elbow); Impingement bet.
heads of FCU
▪ primary fxn loss: 4th & 5th digits for spherical and cylindrical grips, thumb for adduction,
and finger abduction and adduction are lost
▪ deformity: “Claw hand” “Bishop’s/Benediction Hand”
▪ “Cubital Tunnel Syndrome ” “Guyon’s Canal Syndrome”

➢ Radial Nerve Injury (C5 - T1)

▪ Triceps brachii; Anconeus; Brachialis; Brachioradialis; ECRL; ECRB; ECU; EDC; EDQ; Supinator;
APL: EPl; EPB
▪ cause: trauma (elbow hyperextension); humeral fx or penetrating injuries; compression
▪ primary fxn loss: weak supination; unable to make fist or grip objects; triceps cannot push
▪ deformity: “Wrist drop” “Saturday Night Palsy”

XII.DIAGNOSIS

▪ Pt. History (OI; ROM; MMT)

▪ Physical Examination (sensory & motor)
▪ Deep tendon reflexes
▪ Special Tests
✓ Cozen’s Test: the patient is in a sitting position with the forearm is supinated. Palpate the lateral
epicondyle. Ask the patient to actively make a fist, pronate the forearm, and radially deviate and
extend the wrist while the examiner resist the motion. Pain is indicative for lateral epicondylitis.
✓ Tinel Sign (elbow): the patient is in a sitting position. Palpate the area of ulnar nerve. Tingling
sensation in the ulnar nerve distribution of the forearm is indicative for regeneration of the
sensory fibers of a nerve.
✓ Tinel Sign (wrist): the patient is in a sitting position. Tap over the carpal tunnel in the wrist.
Tingling sensation in the ulnar nerve distribution of the forearm is indicative for regeneration of
the sensory fibers of a nerve.
✓ Finkelstein test: the patient is in a sitting position. Ask the patient to make fist then thumb is
inside the fingers then ulnar deviate. Pain in APL and EPB tendons is indicative of De Quervain
Disease.

▪ EMG
✓ Needle records the electrical activity of muscle fibers. Since denervated muscle
fibers display characteristics abnormalities in the needle examination, this part of
the examination is useful in determining the extent such loss and in localizing the
nerve lesions. It can also aid in determining the time of course of the disease to
some extent, as it helps analyzing the process of re-innervation. It is less useful in
evaluating purely demyelinating lesions, as the muscle fibers retain their innervation
in these disorders.

▪ Nerve conduction velocity

✓ Are the most helpful part of the electrodiagnostic examination for peripheral nerve
disorders. These studies determine the conduction velocity of the nerve as well as the
amplitude of the propagated electrical waveform. In motor nerves, the NCV also pro-
vide distal latency information. Both motor and sensory nerves are evaluated by NCV.
DIFFERENTIAL DIAGNOSIS

Occurs after surgery, No CSF affectation

GBS Muscle weakness Are-
viral infection of Occurs in females
flexia Paresthesia
the upper respi- No immune sys-
ratory tract as a tem affectation
result of viral Trauma or disease
antigens trigger- entities
ing an autoim-
mune response
in the body which
leads to weak-
ness and mild
distal sensory
loss
Acute infection Not immune
POLIO Areflexia Atrophy
caused by group mediated
paralysis
of entero viruses
which attacks the Traumatic and non
GIT primarily and traumatic
the Nervous sys-
tem secondarily
PNI is not related to
CMTD Group of heridetary Weakness Muscle atro-
autoimmune
disorders that damage phy paresthesia
dysfunction
the nerve in your arms
CMTD related to
and legs
autoimmune

dysfunction
 XIII. PROGNOSIS
· Nerve conduction deficit is completely reversible in Neuropraxia; recovery begins on aver-
age 6wks post injury as a result of remyelination. It is complete usually.
· There is good prognosis in Axonotmesis although wallerian degeneration occurs distal to the le-
sion. Nerve regeneration is usually effective and proceeds at a rate of about 1 to 2 mm per day.
· Neurotmesis has poor prognosis because of total fiber disruption.

XIV. MEDICAL MANAGE-

MENT For pain:
o Carbamazepine (Tegretol)
o Amitriptyline(Elavil)
o NSAID
o Antiviral medication or corticosteroids can decrease edoneural edema and improve
prognosis

X. SURGICAL MANAGEMENT

· Exploratory Surgery: exposes the extent of the severity of the lesion. Surgery may also be
considered where there is an incomplete loss of function but no improvement over several
weeks or no return of function at about four months after injury. The purpose of surgical
repair is to improve peripheral nerve recovery and eventual function if the prognosis for this
is poor, surgery should not be done.
· Immediate or Primary Repair: is performed within 8 - 12 hours on clean lacerating injuries
· Delayed or Secondary Repair: it is more usual following a major trauma, blunt transection,
or wound contamination, or complete neurotmesis without clear nerve endings, is per-
formed after more than one month. This delay in repair allows better definition of the lesion
and a reduced risk infection.
· Peripheral Nerve Graft: is dine when the segment produces a gap between nerve endings
>2cm.

XV. Physical Therapy Management

In general recovery from nerve injury can be viewed as occurring three phases:
A. Acute Phase: this is early after injury or surgery when the emphasis is on Healing and
Prevention of complications.
▪ Movement: begin ROM to minimize joints and connective contractures and adhesions
▪ Splinting or Bracing
▪ Patient Education: teach patient safe movements and ways to protect the extremity to
avoid injury or loss of sensation
 B. Recovery Phase: when reinnervation occurs. Emphasis is on Training and Re-education.
▪ Motor retraining: AAROM; electrical stimulation
▪ Desensitization: to decrease irritability and increase sensory awareness
▪ Discriminative sensory re-education: process of retraining the brain to recognize stimulus
oncehypersensitivity diminishes
▪ Patient Education: teach preventive care to avoid injury

C. Chronic Phase: occurs when the potential for re-innervation has peaked, and there are
significant residual deficits. Emphasis is Training Compensatory Function.
▪ The patient will probably have to continue to wear supportive devices and preventive care
must continue indefinitely.

Others:
✓ TENS- for temporary relief of pain
✓ ELECTRICAL STIMULATOR - helps re-educate the denervated muscles
✓ HMP- increases blood flow, therefore helps increase in healing effect.
✓ Cold modalities- helps decrease inflammation and pain
✓ ULTRA SOUND - a deep heating modality, this modality can increase extensibility
of structures and aids for healing
✓ Exercise
o ROM
o Strengthening exercise

REFERENCES:
· Colby & Kisner Therapeutic Exercise 6th Edition
· De Lisa’s Physical Medicine and Rehabilitation 5th Edition
· Magee’s Orthopaedic Physical Assessment 6th Edition
· NTG Reviewer 2013 1ST Edition
· https://www.physio-pedia.com/Classification_of_Peripheral_Nerve_Injury